Mutations in four genes that had never before been associated with colorectal cancer have been found to raise a person’s risk for the disease by up to 40% compared with a person not harboring any of these genetic variants.
“These findings could potentially lead to new drug targets and, in combination with previously identified genetic and environmental risk factors, identify subgroups of the population that can benefit most from colorectal cancer screening and could be targeted for early or more frequent endoscopy,” pointed out Ulrike Peters, PhD, MPH, in a statement issued by Fred Hutchinson Cancer Research Center in Seattle, Washington.
Peters, a cancer prevention researcher at Fred Hutchinson, co-led the genome-wide association study that uncovered the new genetic culprits. In this extensive project, detailed in the journal Gastroenterology, the investigative team identified the 10 most statistically significant mutations associated with colorectal cancer out of 2.7 million genetic variants, and further analyzed the 10 variations using 2,098 cases of colorectal cancer, 958 cases of colorectal adenoma, and 6,658 controls of European and Asian descent.
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The researchers uncovered mutations in the following genes:
- Nucleic acid binding protein 1, which is involved in DNA repair
- Laminin gamma 1, which is the second gene in the laminin gene family found to be associated with colorectal cancers
- Cyclin D2, which is involved in cell-cycle control, a key control mechanism in preventing cancer development
- T-box 3, which is a gene transcription factor that targets a known colorectal cancer pathway.
Peters and colleagues found that a person who carries one or two copies of any of these genetic variants has a risk of colorectal cancer 10% to 40% higher than that of a person without these mutations.
